We describe a patient with previously undiagnosed CKD stage 2, who presented at 15+/40 of an IVF pregnancy with severe hypertension and nephrotic syndrome. On renal biopsy, she was found to have TMA without MAHA. FDIU preceded fetal viability and coincided with rapidly escalating renal dysfunction that improved promptly after delivery.
This 49 year old G3P0 underwent IVF in India with a donor egg. She presented to the emergency department at 15+/40 with BP 220/110mmHg requiring intravenous hydralazine and labetalol before being stabilised on oral methyldopa, labetalol and nifedipine. Her serum creatinine at baseline was Cr 74-96 micromol/L with ~10 g/day proteinuria without haematuria. Aspirin and enoxaparin were commenced. Her platelet count and ALT were within normal range. Renal ultrasound showed a small right kidney (with extensive scarring and parenchymal loss on MRI). Her left kidney was normal.
Her obstetric ultrasound at 15+/40 revealed a fetus at the lower limit of normal growth. A renal biopsy 4 weeks later revealed thrombotic microangiopathy with prominent glomerular and arteriolar injury, but no significant chronic parenchymal damage. At 20+/40 a repeat obstetric US revealed extreme fetal growth restriction with EFW 164g and severe oligohydramnios. Within 24 hours, FDIU was documented and her serum creatinine increased from 106 to 213 micromol/L. MgSO4 was commenced due to hyper-reflexia with sustained clonus. Misoprostol induction of labour was complicated with retained products requiring D&C, and Mg toxicity clinically and biochemically (level 4.82mmol/L) requiring iv Ca gluconate. Four days after delivery, her serum creatinine fell to 113 micromol/L and her antihypertensive agents were reduced. Four weeks after delivery, her serum creatinine was 82 micromol/L, albumin 25 g/L and proteinuria 3g/day. Her SLE and APLS serology remained unremarkable.